BLACK FRIDAY SALE:  Save Up to 57% OFF! No Coupon Needed

Defective Mitochondria Connected to Alzheimer’s Disease

Alzheimer’s Disease, which is a progressive neurodegenerative disorder that affects millions of people worldwide, is currently incurable.

Only the symptoms are treatable, and the medical community has poured billions of dollars into clinical trials trying to develop new treatments to slow down the disease.

Yet, while other fields of research such as cancer and HIV therapies made massive leaps in efficacy, new Alzheimer’s drugs continue to flop.

In the last decade plus, the target almost commonly focused on for AD drug development has been amyloid beta plaques and their subsequent elimination.

With an AD brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function.

However, recent research is finding amyloid beta plaque build up is more of a symptom of AD than a cause, and the focus going forward should be on the prevention of such.

Mitochondria A Key Factor In Brain Health

In a new study in the scientific journal, Nature Neuroscience, an international team of researchers from the University of Copenhagen and the University of Oslo among others have come closer to a new way of attacking the disease earlier in a person’s lifespan.

They target the efforts towards the cleaning process in the brain cells called mitophagy.[R]

‘When the cleaning system does not work properly, there will be an accumulation of defective mitochondria in the brain cells. And this may be really dangerous. At any rate, the poor cleaning system is markedly present in cells from both humans and animals with Alzheimer’s. And when we improve the cleaning in live animals, their Alzheimer’s symptoms almost disappear,’ says Vilhelm Bohr, author of the study and affiliate professor at the Center for Healthy Aging and National Institutes of Health.

mitophagy

How Mitophagy Keeps Alzheimer's Disease At Bay

Mitophagy is your body’s way of recycling defective mitochondria, which are the “powerplants” for every cell in the body, to make way for the production of new mitochondria.

Again, with both Alzheimer’s and other states of dementia, there is an accumulation of the proteins tau and beta amyloid in the brain, leading to cell death.

In the new animal models, the researchers show that when boosting mitophagy, such accumulation is slowed down.

In other words, by keeping the brains energy production high the proteins associated with AD are also effectively recycled. 

‘It significantly strengthens our results that the cleaning process seems to be important in both human cells and across different animal species. And then it is encouraging that in living animals we are able to improve the central Alzheimer’s symptoms, memory and learning,’ says Vilhelm Bohr.

This new research adds to the ever growing evidence that mitochondrial health is a key factor in living a disease free life.

More so, that keeping the mitochondria intact and efficient is often at the root of the problem instead of the obvious symptoms most medical treatments are distracted by. 

Share Article

0
Would love your thoughts, please comment.x
()
x

Mito Male Scientific References

1. Cavallini, G., Caracciolo, S., Vitali, G., Modenini, F., & Biagiotti, G. (2004). Carnitine versus androgen administration in the treatment of sexual dysfunction, depressed mood, and fatigue associated with male aging. Urology, 63(4), 641-646. doi:10.1016/j.urology.2003.11.009

2. Malaguarnera, M., Cammalleri, L., Gargante, M. P., Vacante, M., Colonna, V., & Motta, M. (2007). L-Carnitine treatment reduces severity of physical and mental fatigue and increases cognitive functions in centenarians: A randomized and controlled clinical trial. The American Journal of Clinical Nutrition, 86(6), 1738-1744. doi:10.1093/ajcn/86.5.1738

3. Karlic, H., & Lohninger, A. (2004). Supplementation of l-carnitine in athletes: Does it make sense? Nutrition, 20(7-8), 709-715. doi:10.1016/j.nut.2004.04.003


4. Samimi, M., Jamilian, M., Ebrahimi, F. A., Rahimi, M., Tajbakhsh, B., & Asemi, Z. (2016). Oral carnitine supplementation reduces body weight and insulin resistance in women with polycystic ovary syndrome: A randomized, double-blind, placebo-controlled trial. Clinical Endocrinology,84(6), 851-857. doi:10.1111/cen.13003


5. Sahlin, K. (2011). Boosting fat burning with carnitine: An old friend comes out from the shadow. The Journal of Physiology, 589(7), 1509-1510. doi:10.1113/jphysiol.2011.205815


6. Soczynska, J. K., Kennedy, S. H., Chow, C. S., Woldeyohannes, H. O., Konarski, J. Z., & Mcintyre, R. S. (2008). Acetyl-L-carnitine and α-lipoic acid: Possible neurotherapeutic agents for mood disorders? Expert Opinion on Investigational Drugs, 17(6), 827-843. doi:10.1517/13543784.17.6.827


7. Miyagawa, T., Kawamura, H., Obuchi, M., Ikesaki, A., Ozaki, A., Tokunaga, K., . . . Honda, M. (2013). Effects of Oral L-Carnitine Administration in Narcolepsy Patients: A Randomized, Double-Blind, Cross-Over and Placebo-Controlled Trial. PLoS ONE,8(1). doi:10.1371/journal.pone.0053707


8. Cristofano, A., Sapere, N., Marca, G. L., Angiolillo, A., Vitale, M., Corbi, G., . . . Costanzo, A. D. (2016). Serum Levels of Acyl-Carnitines along the Continuum from Normal to Alzheimers Dementia. Plos One, 11(5). doi:10.1371/journal.pone.0155694

. Fillit, H., & Hill, J. (2004). The Economic Benefits of Acetylcholinesterase Inhibitors for Patients with Alzheimer Disease and Associated Dementias. Alzheimer Disease & Associated Disorders,18. doi:10.1097/01.wad.0000127492.65032.d3


10. Miyata, M., Yoshihisa, A., Yamauchi, H., Owada, T., Sato, T., Suzuki, S., . . . Takeishi, Y. (2014). Impact of sleep-disordered breathing on myocardial damage and metabolism in patients with chronic heart failure. Heart and Vessels, 30(3), 318-324. doi:10.1007/s00380-014-0479-6


11. Lango, R. (2001). Influence of ?-carnitine and its derivatives on myocardial metabolism and function in ischemic heart disease and during cardiopulmonary bypass. Cardiovascular Research, 51(1), 21-29. doi:10.1016/s0008-6363(01)00313-3


12. Vescovo, G., Ravara, B., Gobbo, V., Sandri, M., Angelini, A., Barbera, M. D., . . . Libera, L. D. (2002). L-Carnitine: A potential treatment for blocking apoptosis and preventing skeletal muscle myopathy in heart failure. American Journal of Physiology-Cell Physiology, 283(3). doi:10.1152/ajpcell.00046.2002


13. Shadboorestan, A., Shokrzadeh, M., Ahangar, N., Abdollahi, M., Omidi, M., & Payam, S. S. (2013). The chemoprotective effects of l-carnitine against genotoxicity induced by diazinon in rat blood lymphocyte. Toxicology and Industrial Health,31(12), 1334-1340. doi:10.1177/0748233713491811


14. Chowanadisai, W., Bauerly, K. A., Tchaparian, E., Wong, A., Cortopassi, G. A., & Rucker, R. B. (2009). Pyrroloquinoline Quinone Stimulates Mitochondrial Biogenesis through cAMP Response Element-binding Protein Phosphorylation and Increased PGC-1α Expression. Journal of Biological Chemistry,285(1), 142-152. doi:10.1074/jbc.m109.030130


15. Chowanadisai, W., Bauerly, K. A., Tchaparian, E., Wong, A., Cortopassi, G. A., & Rucker, R. B. (2009). Pyrroloquinoline Quinone Stimulates Mitochondrial Biogenesis through cAMP Response Element-binding Protein Phosphorylation and Increased PGC-1α Expression. Journal of Biological Chemistry, 285(1), 142-152. doi:10.1074/jbc.m109.030130


16. Stites TE, Mitchell AE, Rucker RB. Physiological importance of quinoenzymes and the O-quinone family of cofactors. J Nutr. 2000 Apr;130(4):719-27
17. Steinberg, F., Stites, T. E., Anderson, P., Storms, D., Chan, I., Eghbali, S., & Rucker, R. (2003). Pyrroloquinoline Quinone Improves Growth and Reproductive Performance in Mice Fed Chemically Defined Diets. Experimental Biology and Medicine, 228(2), 160-166. doi:10.1177/153537020322800205


18. Biswas, T. K., Pandit, S., Mondal, S., Biswas, S. K., Jana, U., Ghosh, T., . . . Auddy, B. (2010). Clinical evaluation of spermatogenic activity of processed Shilajit in oligospermia. Andrologia,42(1), 48-56. doi:10.1111/j.1439-0272.2009.00956.x


19. Surapaneni, D. K., Adapa, S. R., Preeti, K., Teja, G. R., Veeraragavan, M., & Krishnamurthy, S. (2012). Shilajit attenuates behavioral symptoms of chronic fatigue syndrome by modulating the hypothalamic–pituitary–adrenal axis and mitochondrial bioenergetics in rats. Journal of Ethnopharmacology, 143(1), 91-99. doi:10.1016/j.jep.2012.06.002


20. Chang, C. S., Choi, J. B., Kim, H. J., & Park, S. B. (2011). Correlation Between Serum Testosterone Level and Concentrations of Copper and Zinc in Hair Tissue. Biological Trace Element Research,144(1-3), 264-271. doi:10.1007/s12011-011-9085-y


21. Plasma Steroid-Binding Proteins in Tumour Diseases. (1984). Molecular Aspects of Medicine, 371-380. doi:10.1016/b978-0-08-033239-0.50032-6

[]